Prenatal testosterone exposure decreases aldosterone production but maintains normal plasma volume and increases blood pressure in adult female rats

Amar S. More, Jay S. Mishra, Gary Hankins, Sathish Kumar

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Plasma testosterone levels are elevated in pregnant women with preeclampsia and polycystic ovaries; their offspring are at increased risk for hypertension during adult life. We tested the hypothesis that prenatal testosterone exposure induces dysregulation of the renin-angiotensin-aldosterone system, which is known to play an important role in water and electrolyte balance and blood pressure regulation. Female rats (6 mo old) prenatally exposed to testosterone were examined for adrenal expression of steroidogenic genes, telemetric blood pressure, blood volume and Na+ and K+ levels, plasma aldosterone, angiotensin II and vasopressin levels, and vascular responses to angiotensin II and arg8-vasopressin. The levels of Cyp11b2 (aldosterone synthase), but not the other adrenal steroidogenic genes, were decreased in testosterone females. Accordingly, plasma aldosterone levels were lower in testosterone females. Plasma volume and serum and urine Na+ and K+ levels were not significantly different between control and testosterone females; however, prenatal testosterone exposure significantly increased plasma vasopressin and angiotensin II levels and arterial pressure in adult females. In testosterone females, mesenteric artery contractile responses to angiotensin II were significantly greater, while contractile responses to vasopressin were unaffected. Angiotensin II type-1 receptor expression was increased, while angiotensin II type-2 receptor was decreased in testosterone arteries. These results suggest that prenatal testosterone exposure downregulates adrenal Cyp11b2 expression, leading to decreased plasma aldosterone levels. Elevated angiotensin II and vasopressin levels along with enhanced vascular responsiveness to angiotensin II may serve as an underlying mechanism to maintain plasma volume and Na+ and K+ levels and mediate hypertension in adult testosterone females.

Original languageEnglish (US)
Article number42
JournalBiology of Reproduction
Volume95
Issue number2
DOIs
StatePublished - Aug 1 2016

Fingerprint

Plasma Volume
Aldosterone
Testosterone
Blood Pressure
Angiotensin II
Vasopressins
Blood Vessels
Cytochrome P-450 CYP11B2
Angiotensin Type 2 Receptor
Hypertension
Angiotensin Type 1 Receptor
Mesenteric Arteries
Water-Electrolyte Balance
Renin-Angiotensin System
Pre-Eclampsia
Blood Volume
Pregnant Women
Ovary
Arterial Pressure
Down-Regulation

Keywords

  • AGTR1
  • Aldosterone
  • Angiotensin II
  • Blood pressure
  • Plasma volume
  • Pregnancy
  • Testosterone
  • Vascular function
  • Vasopressin

ASJC Scopus subject areas

  • Cell Biology

Cite this

Prenatal testosterone exposure decreases aldosterone production but maintains normal plasma volume and increases blood pressure in adult female rats. / More, Amar S.; Mishra, Jay S.; Hankins, Gary; Kumar, Sathish.

In: Biology of Reproduction, Vol. 95, No. 2, 42, 01.08.2016.

Research output: Contribution to journalArticle

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